A January study by Czech researchers found at least one thing that affects the permeability of the intestinal mucosa: gut bacteria. Their study may eventually lead to treatment options for human celiacs, by finding ways to protect tender intestines from the harmful effects of gliadin.

Celiac.com 03/15/2011 - For celiacs, it's not really the cinnamon bun that's the enemy. Nor the
pizza crust, nor the ravioli. It's the gliadin in these foods - the
alcohol-soluble portion of the gluten protein - that's the real culprit.

Gliadin is the "gladiator" of the human digestive tract. When
we ingest gliadin, enzymes try to break it down into a form that can be
absorbed by the small intestine. But gliadin resists, fighting hard to
remain intact.

A regular small intestine has, like any good
fortress, a protective wall: the mucosal lining of the intestine. This
layer of mucus normally acts as a barrier against gliadin's assaults.
But in a celiac intestine, the mucosal lining is permeable. With
gliadin's destructive power enhanced by its enzyme sidekick, tissue
Transglutaminase (tTG), it quickly gets past this poorly-guarded layer.

Scientists are working to put their finger on exactly what makes the mucosal lining of a celiac's small intestine so permeable.

Now
a January study by Czech researchers found at least one thing that
affects the permeability of the intestinal mucosa: gut bacteria.

In
this study, called "Role of Intestinal Bacteria in Gliadin-Induced
Changes in Intestinal Mucosa: Study in Germ-Free Rats", researchers tied
off sections of rats' intestines and introduced various kinds of
bacteria to each section. They wanted to measure the effect that these
bacteria had on the intestinal mucus - or more specifically, on the
goblet cells that produce the intestinal mucus. To ensure that the kinds
of bacteria in the rats' intestines were under experimental control,
the rats had been raised from birth in germ-free conditions.

They
found that introducing gliadin to the intestines had the effect of
decreasing the mucus-producing cells, thereby eroding the intestines'
protective layer. No big surprises there - gliadin is a fighter, a
digestive "gladiator", after all.

But when they added strains of
so-called harmful bacteria, Escherichia coli (otherwise known as E coli)
or Shigella, the mucus-producing cells decreased even more. The cells
first secreted massive amounts of mucus, then promptly exhausted
themselves and gave up. This left the intestine looking very similar to
that of a person in the early stages of celiac disease, say the
researchers.

But the tale did indeed have a happy ending. Along
came the good bacteria, Bifidobacterium bifidum (or "Biff" for short).
The mucus-producing cells in the small intestine increased when Biff was
present. In fact, Biff was able to partially reverse the
mucus-decreasing effects of E coli and Shigella.

The researchers
concluded that the composition of gut bacteria has an effect on the
protective mucus of the intestines: an overgrowth of bad bacteria
decreases the protective layer, while the addition of good bacteria
increases the protective layer. Their study may eventually lead to
treatment options for human celiacs, by finding ways to protect tender
intestines from the harmful effects of gliadin.